Abstract | BACKGROUND: METHODS: RESULTS: NO2 production (158 ± 16 and 150 ± 13 pmol/mg protein at baseline in control and APC groups, respectively) was significantly (P < 0.05) increased 1.5 ± 0.1 and 1.4 ± 0.1 fold by APC (n = 4) at 60 and 90 min of reperfusion, respectively, concomitantly, with increased expression of GTPCH-1 (1.3 ± 0.3 fold; n = 5) and eNOS (1.3 ± 0.2 fold; n = 5). In contrast, total NO (NO2 and NO3) was decreased after reperfusion in control experiments. Myocardial infarct size was decreased (43 ± 2% of the area at risk for infarction; n = 6) by APC compared with control experiments (57 ± 1%; n = 6). 2, 4-Diamino-6-hydroxypyrimidine decreased total NO production at baseline (221 ± 25 and 175 ± 31 pmol/mg protein at baseline in control and APC groups, respectively), abolished isoflurane-induced increases in NO at reperfusion, and prevented reductions of myocardial infarct size by APC (60 ± 2%; n = 6). CONCLUSION: APC favorably modulated a NO biosynthetic pathway by up-regulating GTPCH-1 and eNOS, and this action contributed to protection of myocardium against ischemia and reperfusion injury.
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Authors | Ines Baotic, Dorothee Weihrauch, Jesse Procknow, Jeanette Vasquez-Vivar, Zhi-Dong Ge, Shaan Sudhakaran, David C Warltier, Judy R Kersten |
Journal | Anesthesiology
(Anesthesiology)
Vol. 123
Issue 3
Pg. 582-9
(Sep 2015)
ISSN: 1528-1175 [Electronic] United States |
PMID | 26192027
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Anesthetics, Inhalation
- Isoflurane
- Nitric Oxide Synthase Type III
- Nos3 protein, rat
- GTP Cyclohydrolase
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Topics |
- Anesthetics, Inhalation
(administration & dosage)
- Animals
- GTP Cyclohydrolase
(biosynthesis)
- Isoflurane
(administration & dosage)
- Male
- Myocardial Ischemia
(drug therapy, enzymology)
- Myocardial Reperfusion Injury
(drug therapy, enzymology)
- Nitric Oxide Synthase Type III
(biosynthesis)
- Random Allocation
- Rats
- Rats, Wistar
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